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Melatonin as a Medicament for the 24/7 Society: Normal and Pathological Aging

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Book cover Ma Vie en Noir

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Abstract

The levels of enzymes, metabolites, and receptors involved in melatonin synthesis decrease during aging, resulting in low levels of melatonin in the elderly. During aging, free radicals and mitochondrial damage promote oxidative stress in the nervous system because the level of free radical production is higher than that of antioxidants. Oxidative stress leads to cell damage and calcium dysfunction and the levels of inflammatory mediators increase with age, even in the absence of acute infection or physiological stress (so-called inflammaging). Such stress leads to inflammatory damage of cellular components, including proteins, lipids, and DNA, and contributes to the age-related decline in homeostasis efficiency. Reversion of inflammaging by melatonin occurs at different levels, including by the prevention of insulin resistance, suppression of inflammation and downregulation of proinflammatory cytokines, and upregulation of anti-inflammatory ones. In addition to normal aging, protein misfolding, aggregation, and degradation impairment are the main characteristic features of age-related neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Melatonin increases the expression of α- and γ-secretase and decreases β-secretase expression. It also inhibits tau protein phosphorylation. Clinical data support the efficacy of melatonin in the treatment of AD and PD, particularly in the early stages of diseases. Melatonin treatment may also be useful in preventing age-associated bone loss by acting on osteoclasts and osteoblasts and turning the calcium balance positive and by improving sleep.

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  1. Facultad de Ciencias Médicas, Pontificia Univ Católica Argentina, Buenos Aires, Argentina

    Daniel Pedro Cardinali

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Cardinali, D.P. (2016). Melatonin as a Medicament for the 24/7 Society: Normal and Pathological Aging. In: Ma Vie en Noir. Springer Biographies. Springer, Cham. https://doi.org/10.1007/978-3-319-41679-3_13

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